In patients with vitiligo, the white patches greatly affect their quality of life (Ongenae et al. 2006). Vitiligo may seem a minor disorder on first sight, but, people with severe depigmentation may have troubles in dating (Papadopoulos et al. 1999) or self-esteem or social activities psychologically (Kent et al. 1996). Therefore, modification of skin pigmentation using whitening agents and coloring agents has gained a lot of attention in the field of pharmacology and cosmeceuticals (Michaela and Vincent 2008).
Melanin is secreted by melanocytes found in the basal layer of the dermis (Kim and Uyama 2005). Upon biosynthesis by the melanocytes differentiating in the neural crest, melanin is transferred to the epidermis by keratinocytes (Yaar et al. 2006). The melanocyte has a specialized organelle called melanosome, which regulates melanin production and contains various enzymes (Tiedtke et al. 2004). Melanin plays important roles of protecting the skin from harmful effects by absorbing UV, removing reactive oxygen species and scavenging toxic drugs and chemicals (Yaar et al. 2006).
Melanin synthesis is catalyzed by tyrosinase-related protein 1 (TRP1) and tyrosinase-related protein 2 (TRP2 or DCT) (Huang et al. 2008). In the skin exposed to UV radiation, melanin synthesis is initiated by the enzyme tyrosinase (Parvez et al. 2006). Tyrosinase, which is known as an important enzyme that catalyzes melanin synthesis in the melanocytes (Sturm et al. 2000), plays an important role in oxidizing tyrosine to DOPA and DOPA to dopaquinone (Tripathi et al. 1992). Dopaquinone is spontaneously converted to dopachrome. TRP2 (DCT) catalyzes the conversion of dopachrome to DHICA, and TRP1 catalyzes the oxidation of DHICA to indole-5,6-quinone-2-carboxylic acid (Kim and Uyama 2005).
Vitiligo is a depigmentation condition characterized by localized depigmented patches caused by loss of melanin in the epidermis or functional inability of melanocytes (Helen et al. 2007). In order to explain the dysfunction of melanocytes in the epidermis, the autoimmune mechanism, the autocytotoxic mechanism and the hypothesis that abnormal melanocytes nearby keratinocytes lose their function are presented (Ongenae 2003; Moretti 2002). Other causes of vitiligo include stress, infection, genetic factors, melatonin receptors, and migration and proliferation of damaged melanocytes (Helen et al. 2007). 3-Isobutyl-1-methylxanthine (IBMX), which is a strong stimulant of melanin synthesis (David 2001), increases cAMP content in cells by inhibiting cAMP phosphodiesterase (Im et al. 1998), and dibutyryl cAMP increases tyrosinase activity and mRNA expression (Hoganson et al 1989). MITF is a master regulator of melanocyte development and melanin synthesis (Levy et al. 2006) and regulates transcription of the major pigmentation enzymes, tyrosinase, TRP-1 and TRP-2 (Koo et al. 2008).
At present, topical application of corticosteroid, calcineurin inhibitor, vitamin D derivatives, phototherapy (UVA, narrowband UVB, photochemical therapy), surgery, and a combination of topical treatment and phototherapy are tried for the treatment of vitiligo (Maxine et al. 2008). It is reported that the patients who refuse the photochemical therapy have increased incidence of non-melanoma and melanoma skin cancer (Rajatanavin et al. 2003). Accordingly, efforts are made to find natural substances for development of new skin care medicines and the use of natural substances in skin care cosmetics is becoming more important (Kiken et al. 2002).
Canities (hair graying) is caused by decreased tyrosinase activity of hair bulbar melanocytes due to toxic oxidation of the melanocytes and defective migration of the melanocytes from the reservoir in the upper outer root sheath to the pigment-permitting microenvironment close to the dermal papilla (Neste and Tobin 2004; Tobin et al. 2001). Canities is one of the typical signs of human aging and the maintenance of hair color depends on the consistent presence of melanocytes and retention of their function (Kerscher et al. 2007; Lin and Fisher 2007; Sarin et al. 2007). Melanocyte stem cells (MSCs) were found in the hair follicle. Unlike epithelial melanocytes, hair follicle melanocytes are produced in the early stage of each hair cycle and undergo apoptosis at the end thereof. When the cycle repeats 7-15 times over 45 years or longer, the hair follicle cannot produce melanin any more. Since the hair follows the regular cycling/re-pigmentation processes during lifetime, the gradual loss of hair color with aging in animals including human and mouse suggests that the canities may be caused by the damaged self-maintenance ability of the MSCs.
Plant compounds known to have useful activities are utilized in the manufacture of cosmetics (Huang et al. 2008). The flower and flower bud of Sophora japonica are well known as traditional medicinal herb in China (Loa et al. 2009) and have antitumor, antisterilic and anticancer activities (Ma 2006; Wang 2001). The ingredients of Sophora japonica include flavonol triglucoside, isoflavonol, cumaronchromone, saponin, triterpene glucoside, phospholipid, alkaloid, amino acid, polysaccharide and fatty acid (Grupp et al. 2001). Sophora japonica extract is usually used to treat hemorrhage-related disorders such as bloody excrement, rectal hemorrhage, uterine hemorrhage and diarrhea (Zhao 2004).
Throughout the specification, a number of publications and patent documents are referred to and cited. The disclosure of the cited publications and patent documents is incorporated herein by reference in its entirety to more clearly describe the state of the related art and the present disclosure.